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In situ assessment of the rat heart during chronic carbon monoxide exposure using nuclear magnetic resonance imaging
Author(s) -
Bambach Gregory A.,
Penney David G.,
Negendank William G.
Publication year - 1991
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550110109
Subject(s) - ventricle , carboxyhemoglobin , hematocrit , interventricular septum , chemistry , medicine , magnetic resonance imaging , muscle hypertrophy , nuclear medicine , cardiology , carbon monoxide , radiology , biochemistry , catalysis
Ventricular hypertrophy induced in male Sprague‐Dawley rats by inhalation of 500 ppm carbon monoxide (40% carboxyhemoglobin level) for 0–62 days was assessed by contiguous 2‐mm thick axial cardiac crosssections, using 32 accumulated averages of ungated fast‐scan gradient‐recalled nuclear magnetic resonance (NMR) images. Following final imaging, the rats were sacrificed and the hematocrit and heart mass were determined. The mean outside diameter of the left ventricle plus interventricular septum (LV + S) showed a strong correlation ( r = 0.73, P <0.01) with the duration of CO exposure, while the correlation coefficients for the LV + S Iumen diameter and wall thickness were marginally significant. The mean pleural space diameter also increased significantly ( r = 0.64, P <0.05) with the duration of CO exposure. The ratio of LV + S wall thickness and the Iumen radius was 0.53 in the rats exposed to CO for 0–8 days; this value did not change with longer CO exposure. The LV + S outside and Iumen diameter showed significant correlations to the hematocrit ( r = 0.72, p <0.05 and r = 0.66, P <0.05, respectively), and the LV + S outside diameter correlated with the increase in the LV + S mass ( r = 0.72, P <0.05). The results achieved with NMR imaging are consistent with past morphometric studies of CO‐induced ventricular hypertrophy, where heart dimensions were determined in relaxed frozen tissue, and corroborate the eccentric nature of CO‐induced ventricular hypertrophy.